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Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway

Mounting evidence indicates that there exists an association between heparanase (HPSE) and several physiological and pathological mechanisms in humans. However, the dynamics of the mechanisms involved in the regulation of HPSE expression in pancreatic cancer (PC) remain unclear. The aim of the prese...

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Autores principales: Wang, Cheng, Wei, Yajun, Wang, Gang, Zhou, Yangming, Zhang, Jingcheng, Xu, Kai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7336506/
https://www.ncbi.nlm.nih.gov/pubmed/32627022
http://dx.doi.org/10.3892/or.2020.7641
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author Wang, Cheng
Wei, Yajun
Wang, Gang
Zhou, Yangming
Zhang, Jingcheng
Xu, Kai
author_facet Wang, Cheng
Wei, Yajun
Wang, Gang
Zhou, Yangming
Zhang, Jingcheng
Xu, Kai
author_sort Wang, Cheng
collection PubMed
description Mounting evidence indicates that there exists an association between heparanase (HPSE) and several physiological and pathological mechanisms in humans. However, the dynamics of the mechanisms involved in the regulation of HPSE expression in pancreatic cancer (PC) remain unclear. The aim of the present study was to assess the levels of HPSE in PC tissues and cell lines by western blotting and reverse transcription-quantitative PCR (RT-qPCR) analysis. Wound healing and Transwell assays were conducted to examine the effects of HPSE on migration and invasion in sh-NC and sh-HPSE PC cell lines. In addition, tumor growth was assessed in a mouse xenograft model in vivo. The expression levels of epithelial-to-mesenchymal transition (EMT)-related biomarkers and the involvement of the Wnt/β-catenin pathway were assessed by analyzing the results of western blot and RT-qPCR assays. The results indicated that the expression of HPSE was substantially higher in PC tissues and cell lines, whereas experimental knockdown of HPSE suppressed the rates of migration and invasion of PC cells. Western blotting was used to assess the expression of EMT biomarkers and determine the function of HPSE in EMT. Furthermore, our results indicated that downregulation of HPSE expression decreased the expression of Wnt/β-catenin associated proteins. In conclusion, HPSE appears to be a good candidate as a molecular target for the treatment of PC based on the finding of the present study.
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spelling pubmed-73365062020-07-07 Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway Wang, Cheng Wei, Yajun Wang, Gang Zhou, Yangming Zhang, Jingcheng Xu, Kai Oncol Rep Articles Mounting evidence indicates that there exists an association between heparanase (HPSE) and several physiological and pathological mechanisms in humans. However, the dynamics of the mechanisms involved in the regulation of HPSE expression in pancreatic cancer (PC) remain unclear. The aim of the present study was to assess the levels of HPSE in PC tissues and cell lines by western blotting and reverse transcription-quantitative PCR (RT-qPCR) analysis. Wound healing and Transwell assays were conducted to examine the effects of HPSE on migration and invasion in sh-NC and sh-HPSE PC cell lines. In addition, tumor growth was assessed in a mouse xenograft model in vivo. The expression levels of epithelial-to-mesenchymal transition (EMT)-related biomarkers and the involvement of the Wnt/β-catenin pathway were assessed by analyzing the results of western blot and RT-qPCR assays. The results indicated that the expression of HPSE was substantially higher in PC tissues and cell lines, whereas experimental knockdown of HPSE suppressed the rates of migration and invasion of PC cells. Western blotting was used to assess the expression of EMT biomarkers and determine the function of HPSE in EMT. Furthermore, our results indicated that downregulation of HPSE expression decreased the expression of Wnt/β-catenin associated proteins. In conclusion, HPSE appears to be a good candidate as a molecular target for the treatment of PC based on the finding of the present study. D.A. Spandidos 2020-08 2020-06-10 /pmc/articles/PMC7336506/ /pubmed/32627022 http://dx.doi.org/10.3892/or.2020.7641 Text en Copyright: © Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Wang, Cheng
Wei, Yajun
Wang, Gang
Zhou, Yangming
Zhang, Jingcheng
Xu, Kai
Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway
title Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway
title_full Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway
title_fullStr Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway
title_full_unstemmed Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway
title_short Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the Wnt/β-catenin pathway
title_sort heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial-to-mesenchymal transition through the wnt/β-catenin pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7336506/
https://www.ncbi.nlm.nih.gov/pubmed/32627022
http://dx.doi.org/10.3892/or.2020.7641
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